Patho Exam 2 (Ch. 9, 12, 14, 15, 16)

First line of defense

Mechanical barriers and secretions: unbroken skin and mucous membranes; tears, sweat, and gastric juice

Second line of defense

Non-specific defenses: phagocytosis, inflammation, and interferon

Interferon

Cytokines that stop viral replication

Third line of defense

Specific defense: specific antibodies

Inflammation

Normal, protective defense mechanism; its signs and symptoms warn of an underlying problem

Causes of inflammation

Cuts, fractures, chemicals, ischemia or infarction, allergies, foreign bodies, and infection

Acute inflammation

Self-limited and of short duration; chemical mediators released in injured tissue affect blood vessels and nerves and initiate the vascular and cellular phases; involves exudate formation and transmigration of neutrophils and monocytes

Vascular phase

Changes in blood flow and vascular permeability

Vasodilation

Increased blood flow to the damaged site, caused by chemical mediators

Hyperemia

Higher-than-normal blood flow

Leakage of exudate

Provides a protein-rich environment to fight further infection

Cellular phase

Recruitment and cleaning by phagocytes

Margination and rolling

Peripheral positioning of leukocytes along the vessel wall during inflammation; rolling is the repeated connection to and disconnection from the endothelium

Adhesion

High-affinity integrin binding that stops rolling

Transmigration

Squeezing of leukocytes through the tight vessel wall

Phagocytosis

Neutrophils and macrophages engulf and destroy pathogens

Histamine

Chemical mediator released from mast cells; causes vasodilation and increased vascular permeability

Cytokines

Signaling proteins released by cells such as leukocytes that regulate the inflammatory and immune response

Interleukins

Cytokines produced by leukocytes that act on other leukocytes; promote inflammation and act as pyrogens

Lymphokines

Cytokines released by lymphocytes that activate other immune cells such as macrophages

Leukotrienes

Lipid mediators made from arachidonic acid by lipoxygenase; increase vascular permeability and attract leukocytes

Prostaglandins

Lipid mediators made from arachidonic acid by cyclooxygenase; cause vasodilation, pain, and fever

Bradykinin

Peptide mediator that causes vasodilation, increased vascular permeability, and pain

Arachidonic acid

Fatty acid released from injured cell membranes; precursor of leukotrienes and prostaglandins

Lipoxygenase

Enzyme that synthesizes leukotrienes

Cyclooxygenase

Enzyme that synthesizes prostaglandins

Calor

Redness and warmth

Tumor

Swelling

Dolor

Pain

Functio laesa

Loss of function

Exudate

Fluid that leaks from capillaries into the interstitial space during inflammation

Serous exudate

Watery exudate due to viral infection; consists of fluid, protein, and WBCs

Hemorrhagic exudate

Contains RBCs due to rupture of blood vessels

Fibrinous exudate

High in fibrin from fibrin clots; sticky and thick

Membranous exudate

Develops on membrane surfaces; gray and white; necrotic cells with fibrin

Purulent exudate

Contains a large amount of pus

Fever (pyrexia)

Common with inflammation; triggered by pyrogens that reset the thermoregulatory center

Pyrogens

Interleukins and tumor necrosis factor, released by leukocytes, that trigger fever

Intermittent fever

Temperature fluctuates high and low from hour to hour

Sustained fever

Consistently high fever

Remittent fever

Same as intermittent, but the temperature goes down less

Relapsing fever

Fever highest in the morning and evening

Leukocytosis

Increased WBC count, bone marrow activity, and release of leukocytes

Erythrocyte sedimentation rate

Increased plasma proteins cause RBCs to settle faster

Differential WBC count

Percentage of each WBC type in the blood

Chronic inflammation

Lasts 2+ weeks; due to unsuccessful acute inflammation; increased infiltration of lymphocytes, macrophages, and fibroblasts; a granuloma may develop around a foreign object

Granuloma

Cluster of immune cells that walls off a pathogen that cannot be eliminated; contains giant and epithelioid cells; associated with foreign bodies and microorganisms

Labile cells

Continue to divide and replicate throughout life

Stable cells

Normally stop dividing when growth ceases (e.g., bone cells)

Permanent cells

Don't divide (e.g., neurons)

Resolution

Type of healing in which damaged cells recover

Regeneration

Type of healing in which damaged tissue is replaced by the same type of cells

Replacement or fibrosis

Damaged tissue is replaced by scar tissue; results in downgrade of function

Innate immunity

Non-specific defense present from birth; responds immediately and the same way each time (phagocytes, inflammation mediators, complement)

Adaptive (specific) immunity

Very specific response that must be "primed"; slower the first time, immediate and robust on re-exposure; involves B and T lymphocytes

Humoral immunity

Adaptive immunity mediated by B lymphocytes, which produce antibodies against pathogens and toxins

Cell-mediated immunity (CMI)

Adaptive immunity mediated by T lymphocytes, which destroy infected or abnormal cells and coordinate immune responses

Phagocytes

Innate immune cells (neutrophils, macrophages) that engulf and destroy pathogens

Innate inflammation mediators

Cytokines, prostaglandins, complement, and histamine

Antigen

Substance that triggers an immune response in the body

Self antigen

HLA proteins that label a person's own cells; the immune system ignores them

Non-self antigen

Foreign antigen recognized by the immune system, leading to a specific response and memory cell production

Memory cells

Cells produced after antigen exposure that allow a quick response on re-exposure

Antibody (immunoglobulin)

Protein produced by plasma cells that identifies and neutralizes foreign antigens

Neutralization

Antibody function in which the antibody directly blocks the antigen

Opsonization

Antibody marks a pathogen for removal by macrophages

Complement activation

Antibodies bind complement proteins, activating the MAC, which punches holes in foreign cell membranes

MAC (membrane attack complex)

Complement complex that destroys foreign cells by punching holes in their membranes

IgG

Most common antibody in blood; produced during the secondary immune response

IgM

First antibody to increase; produced during the primary immune response

IgA

Antibody common in secretions (tears, saliva, breast milk)

IgE

Antibody responsible for allergic responses and parasitic infections

IgD

Antibody that helps activate B cells

B cells

Lymphocytes that mature in bone marrow and become plasma cells and memory B cells

T cells

Lymphocytes that mature in the thymus; types include helper, memory, suppressor, and cytotoxic T cells

Plasma cells

Activated B cells that produce antibodies

Helper T cell (CD4)

T cell needed for antigen stimulation of B cells; recognizes MHC type II; the cell destroyed by HIV

Cytotoxic T cell (CD8)

T cell that kills infected or abnormal cells; recognizes MHC type I

Major histocompatibility complex (MHC)

Also called HLA; set of molecules on cell surfaces that controls the immune response through recognition of self and non-self; unique to each person

Human leukocyte antigen (HLA)

Another name for MHC; genes code for it, and it is responsible for antigen presentation and lymphocyte recognition

MHC type I

Receptors recognized by CD8 (cytotoxic) T cells

MHC type II

Receptors recognized by CD4 (helper) T cells

Graft

A cell, tissue, or organ transplanted to replace damaged tissue

Allogeneic graft (allograft)

Donor and recipient are related or unrelated but share similar HLA types

Syngeneic graft

Donor and recipient are identical twins

Autologous graft (autograft)

Donor and recipient are the same person

Stem cell transplantation

Allogeneic transplant from an unaffected donor that can cure primary immunodeficiencies caused by stem cell deficiency (e.g., SCID, Wiskott-Aldrich syndrome)

Myeloablative chemotherapy

High-dose chemotherapy that destroys the host's bone marrow cells before stem cell transplant so donor stem cells can repopulate it

Transplant rejection

Recipient's immune system attacks a transplanted organ or tissue because of HLA differences

Hyperacute rejection

Antibody-mediated rejection within minutes to hours of transplant; caused by pre-existing recipient antibodies to graft antigens (type III hypersensitivity per slides)

Acute rejection

Cell-mediated (T lymphocyte) rejection within the first few months, with signs of organ failure; may also occur months or years later if immunosuppression is stopped

Chronic rejection

Rejection after a prolonged period from immune-mediated inflammatory graft injury; unclear mechanism; causes dense fibrosis and progressive decline in organ function

Graft-versus-host disease (GVHD)

Donor T cells in an allogeneic transplant recognize host HLA as foreign and attack host cells; common after allogeneic bone marrow transplant

Requirements for GVHD

Graft has functional cellular immune component; recipient tissues bear antigens foreign to donor cells; recipient immunity is too compromised to destroy donor cells

Acute GVHD

GVHD occurring within 100 days of transplantation

Chronic GVHD

GVHD occurring after 100 days from transplantation

GVHD vs. transplant rejection

In GVHD, immunocompetent donor cells attack an immunocompromised recipient; in rejection, the recipient's immune system attacks the transplanted organ

Hypersensitivity

Exaggerated or inappropriate immune response to an antigen that causes tissue damage; classified into types I to IV

Type I hypersensitivity

Immediate, IgE-mediated allergic reaction within minutes of re-exposure to an allergen; mast cell degranulation (e.g., hay fever, skin rashes, asthma, anaphylaxis)

Allergen

Antigen that triggers an allergic reaction